Park In Ho, Geno K Aaron, Sherwood Logan K, Nahm Moon H, Beall Bernard
Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Respiratory Diseases Branch, Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America.
PLoS One. 2014 May 15;9(5):e97825. doi: 10.1371/journal.pone.0097825. eCollection 2014.
Since nasopharyngeal carriage of pneumococcus precedes invasive pneumococcal disease, characteristics of carriage isolates could be incorrectly assumed to reflect those of invasive isolates. While most pneumococci express a capsular polysaccharide, nontypeable pneumococci are sometimes isolated. Carriage nontypeables tend to encode novel surface proteins in place of a capsular polysaccharide synthetic locus, the cps locus. In contrast, capsular polysaccharide is believed to be indispensable for invasive pneumococcal disease, and nontypeables from population-based invasive pneumococcal disease surveillance have not been extensively characterized. We received 14,328 invasive pneumococcal isolates through the Active Bacterial Core surveillance program during 2006-2009. Isolates that were nontypeable by Quellung serotyping were characterized by PCR serotyping, sequence analyses of the cps locus, and multilocus sequence typing. Eighty-eight isolates were Quellung-nontypeable (0.61%). Of these, 79 (89.8%) contained cps loci. Twenty-two nontypeables exhibited serotype 8 cps loci with defects, primarily within wchA. Six of the remaining nine isolates contained previously-described aliB homologs in place of cps loci. Multilocus sequence typing revealed that most nontypeables that lacked capsular biosynthetic genes were related to established non-encapsulated lineages. Thus, invasive pneumococcal disease caused by nontypeable pneumococcus remains rare in the United States, and while carriage nontypeables lacking cps loci are frequently isolated, such nontypeable are extremely rare in invasive pneumococcal disease. Most invasive nontypeable pneumococci possess defective cps locus genes, with an over-representation of defective serotype 8 cps variants.
由于肺炎球菌的鼻咽部携带先于侵袭性肺炎球菌疾病，因此可能会错误地认为携带菌株的特征反映了侵袭性菌株的特征。虽然大多数肺炎球菌表达荚膜多糖，但有时也会分离出不可分型的肺炎球菌。携带的不可分型菌株往往编码新的表面蛋白来取代荚膜多糖合成位点，即cps位点。相比之下，荚膜多糖被认为是侵袭性肺炎球菌疾病不可或缺的，而基于人群的侵袭性肺炎球菌疾病监测中分离出的不可分型菌株尚未得到广泛的特征描述。在2006 - 2009年期间，我们通过主动细菌核心监测项目收到了14328株侵袭性肺炎球菌分离株。通过荚膜肿胀试验血清分型不可分型的分离株，采用PCR血清分型、cps位点序列分析和多位点序列分型进行特征描述。88株分离株荚膜肿胀试验不可分型（0.61%）。其中，79株（89.8%）含有cps位点。22株不可分型菌株表现出8型cps位点存在缺陷，主要在wchA内。其余9株分离株中的6株含有先前描述的aliB同源物来取代cps位点。多位点序列分型显示，大多数缺乏荚膜生物合成基因的不可分型菌株与已确定的非包膜谱系有关。因此，在美国，由不可分型肺炎球菌引起的侵袭性肺炎球菌疾病仍然很少见；虽然经常分离出缺乏cps位点的携带不可分型菌株，但这种不可分型菌株在侵袭性肺炎球菌疾病中极为罕见。大多数侵袭性不可分型肺炎球菌具有有缺陷的cps位点基因，其中8型cps变异体缺陷的比例过高。
